title: ACTH-induced cortisol secretion is mediated by cAMP and PKC in various adrenocortical adenomas.
abstract: We examined the role of PKC in cortisol secretion from adrenocortical adenomas. Isolated cells were prepared from aldosterone producing adenoma (APA, n=5), APA complicated with pre-clinical Cushing's syndrome (APA+PC, n=1), PC (n=2), and cortisol producing adenoma (CPA, n=5). They were stimulated with 100 nM ACTH, 1 microM forskolin (FS), 1 microM tetradecanoyl phorbol 13-acetate (TPA), and 100 nM angiotensin II (AngII). ACTH was most potent to secret cortisol. FS also stimulated cortisol secretion, but did less-potently. TPA and AngII also stimulated cortisol secretion significantly in cells from CPA. Furthermore, ACTH- and TPA-induced PKCalpha and beta translocations from cytosol to membrane were observed in adenoma cells from APA+PC, PC, and CPA. In conclusion, it was suggested that ACTH-induced cortisol secretion may be mediated by both PKC and protein kinase A in adrenocortical adenomas, and that PKC-mediated signal transduction may be involved in ACTH-induced cortisol secretion in CPA.
authors.affiliation: The Third Department of Internal Medicine, Gifu University School of Medicine, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Ishizuka
authors.forename: H
authors.initials: H
authors.lastname: Daidoh
authors.forename: H
authors.initials: H
authors.lastname: Morita
authors.forename: T
authors.initials: T
authors.lastname: Mune
authors.forename: A
authors.initials: A
authors.lastname: Miura
authors.forename: T
authors.initials: T
authors.lastname: Suwa
authors.forename: T
authors.initials: T
authors.lastname: Shibata
authors.forename: K
authors.initials: K
authors.lastname: Yamada
authors.forename: S
authors.initials: S
authors.lastname: Itaya
authors.forename: K
authors.initials: K
authors.lastname: Kajita
authors.forename: K
authors.initials: K
authors.lastname: Yasuda
mesh_terms: D000236:Adenoma / Q000378:metabolism* / Q000473:pathology; D000306:Adrenal Cortex Neoplasms / Q000378:metabolism* / Q000473:pathology; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000378:metabolism; D000804:Angiotensin II / Q000494:pharmacology; D005576:Colforsin / Q000494:pharmacology; D003480:Cushing Syndrome / Q000378:metabolism* / Q000473:pathology; D000242:Cyclic AMP / Q000378:metabolism*; D003600:Cytosol / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism*; D015151:Immunoblotting; D008297:Male; D008565:Membrane Proteins / Q000187:drug effects / Q000378:metabolism; D008875:Middle Aged; D011493:Protein Kinase C / Q000187:drug effects / Q000378:metabolism*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D013997:Time Factors; D014407:Tumor Cells, Cultured
chemical_list: D008565:Membrane Proteins; D000804:Angiotensin II; D005576:Colforsin; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D000242:Cyclic AMP; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate; D006854:Hydrocortisone